9 peripheral artery disease

7/27/2019 9 Peripheral Artery Disease

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9: Peripheral Artery Disease

Overview

This chapter summarizes pertinent information regarding peripheral arterial disease (PAD) affecting the upper and lower

extremities, renal circulation and visceral vessels. PAD has assumed increasing importance in comprehensive CV care.

Authors

Patrick T. O'Gara, MD, FACC

Editor-in-Chief

Thomas M. Bashore, MD, FACC

Associate Editor

James C. Fang, MD, FACCAssociate Editor

Glenn A. Hirsch, MD, MHS, FACC

Associate Editor

Julia H. Indik, MD, PhD, FACC

Associate Editor

Donna M. Polk, MD, MPH, FACC

Associate Editor

Sunil V. Rao, MD, FACC

Associate Editor


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Introduction

PAD is primarily the result of atherosclerosis in the arteries of the lower extremities, and is frequently associated with

atherosclerosis in all vascular distributions. As a result, the presence of PAD confers a significant risk of cardiovascular

morbidity and mortality, primarily due to stroke (from cerebrovascular atherosclerosis) and myocardial infarction (MI from

coronary atherosclerosis). The astute recognition of PAD therefore provides a unique opportunity to identify individuals at

high risk for adverse cardiovascular events, treat systemic atherosclerosis, and improve cardiovascular outcomes.


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Epidemiology

The prevalence of PAD increases with advancing age. In the United States, 3% of individuals 40-59 years old have an

abnormal ankle-brachial index (ABI), indicative of PAD 8% of those 60-69 and 19% of those >70 years old also are

afflicted, with a total of 8.4 million individuals in the country with PAD. 1, 2

In addition to increasing age, the risk factors responsible for PAD are similar to those for coronary artery disease:

diabetes, tobacco use, hypertension, and dyslipidemia have the strongest impact. Diabetes and tobacco use each confer

a threefold to fourfold increase in the risk of developing PAD. Unlike coronary disease, however, in population-based

studies, the prevalence of PAD is equal in men and women.3, 4


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Diagnosis

Most often, PAD is either clinical silent or is manifest as intermittent claudication

(IC). Classic IC was originally described by Rose and is characterized by:

Exertionally associated calf pain.

Pain that is relieved within 10 minutes of rest.

Pain that does not come on at rest.

Of note, only 10-30% of patients with PAD experience classic IC symptoms. It isestimated that 25-60% of patients with PAD are asymptomatic.

The two most common classification schemes for PAD are the Rutherford and

Fontaine classifications (Tables 1, 2).

In more severe cases, PAD may progress to include pain at rest, skin breakdown or

ulceration, and gangrene, three hallmark findings of critical limb ischemia (CLI).

Patients with advanced PAD may describe a pain, ache, or numbness in the leg at

rest, worsened with elevation of the leg, and relieved with dependent positioning,

such as dangling the leg off the edge of the bed.

Physical examination for PAD may disclose:

Diminished or absent pulses.Bruits (carotid, supraclavicular, abdominal, femoral).

Muscle atrophy.

Dependent rubor and elevation pallor of the feet.

Signs of CLI: hair loss, smooth/shiny skin, dystrophic nails, coolness, pallor,

or cyanosis of the foot.

In evaluating patients with possible PAD, it is important to differentiate between other

processes with similar symptom profiles. Degenerative disc disease or spinal

stenosis may manifest similar leg pain with exertion (pseudoclaudication). In some

instances, patients may describe pain that persists while standing still or pain that

is relieved while continuing to walk, leaning forward over a shopping cart. Such

symptoms are less characteristic of PAD and more likely indicative of

pseudoclaudication. Diabetic neuropathy, deconditioning, and muscular strain are

other entities that may be difficult to distinguish from PAD.

Perhaps the most useful and cost-effective tool to diagnose PAD is the ABI ( Figure

1). The study is performed by applying a blood pressure (BP) cuff to the calf and then

measuring BP at the ankle using a continuous-wave Doppler probe. The higher of

the dorsalis pedis or posterior tibial artery pressures is recorded as the ankle

pressure. The process is repeated with the cuff on the biceps and the Doppler on

the brachial artery, quantifying the brachial pressure. The ABI is then calculated by

dividing the ankle pressure by the higher of the two brachial pressures.

In healthy individuals, the ankle pressure should be higher than the brachial

pressure, with a resulting ABI of 0.9-1.3. If the ankle pressure is >10% lower than the

brachial pressure (i.e., ABI


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with exertion may unmask or accentuate the hemodynamic impact of arterial

stenosis, which may be subtle on resting ABI.

The exercise program provides a universal yardstick to evaluate functional

capacity and may be a handy measure of performance pre- and post-

revascularization.

Exercise may uncover occult coronary disease or angina pectoris.

For its roles in identifying patients with PAD, discriminating claudication from

pseudoclaudication, and assessing functional capacity, exercise treadmill testing

with ABI receives a Class I indication in theAmerican College of Cardiology

(ACC)/American Heart Association (AHA) 2005 Practice Guidelines for the

Management of Patients With PAD.5

Segmental limb pressures, analogous to the ABI, assess the BP at sequentially

more distal loci along the length of the leg: thigh, calf, ankle, transmetatarsal, and

digit. Identifying the location in the leg where the BP abruptly diminishes relative to

the brachial pressure, one may determine the level at which the arterial obstruction

occurs.

Pulse volume recording (plethysmography) provides a noninvasive assessment of

the arterial waveform at sequential loci along the leg. Identifying areas where the

amplitude of the waveform becomes diminished, and where the contour of the

waveform becomes blunted and spread out, may provide insight into the presence

and severity of obstruction at the immediately adjacent and proximal arterial

segments.

Noninvasive anatomic imaging studies, including duplex ultrasonography, magnetic

resonance angiography, and computed tomographic angiography, may provide an

exquisite roadmap of the vasculature if revascularization is being considered. These

studies, however, are not the first-line approach to making the original diagnosis of

PAD.

Invasive angiography represents the gold standard for anatomic imaging. In cases

where an arterial stenosis is of indeterminate severity, hemodynamic evaluation

may be considered by measuring a pressure gradient across the lesion. The utility

of invasive pressure wire assessment is being validated in various arterial

distributions as well. Intraluminal anatomic visualization also may be performed with

intravascular ultrasound. At present, optical coherence tomography has not been

studied extensively in the periphery, and invasive angioscopy remains primarily a

research tool.


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Rutherford Classification Scheme for Peripheral Arterial Disease

Table 1


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Fontaine Classification Scheme

Table 2


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Ankle-Brachial Index

Figure 1

ABI = ankle-brachial index DP = dorsalis pedis PT = posterior tibial.

Adapted with permission from Hiatt WR. Medical treatment of peripheral arterial disease and claudication. N Engl J Med 2001344:1608-21.


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Natural History

In most of patients diagnosed with PAD, the outcomes with respect to the limb are

ironically less morbid than the systemic manifestations of panvascular

atherosclerosis. Specifically, for patients who present with claudication, the majority

(73%) will have stable symptoms over the ensuing 5 years. While 16% may have

progressive claudication, only 7% will require surgical revascularization and 4% will

require amputation.6 Predictors of progressive PAD include diabetes, tobacco use,

ABI


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Public Awareness

A major impediment to the appropriate treatment of PAD is that the disease remains

under-recognized by the public and the clinical implications of the diagnosis are

underappreciated even within the medical community. The mortality of PAD exceeds

that of breast cancer or Hodgkin's disease, and is just below that of colon cancer

(Figure 3).8

In a telephone survey of 2,501 Americans >50 years, only 26% were "very" or

"somewhat" familiar with what PAD is. A higher percentage of individuals surveyed

recognized cystic fibrosis (29%), Lou Gehrig's disease (amyotrophic lateral

sclerosis [ALS], 36%), and multiple sclerosis (42%). Comparatively, however, while

PAD affects nearly 9 million individuals in the United States, cystic fibrosis affects

30,000, ALS affects 20,000, and multiple sclerosis affects 300,000. Improved public

awareness of PAD is paramount, given its high prevalence and profound morbidity

is paramount.9

Figure 3

Five-Year Mortality of Peripheral Arterial Disease vs. Common Types of Cancer

Figure 3

PAD = peripheral arterial disease.

Reproduced with permission from Criqui MH. Systemic atherosclerosis risk and the mandate for intervention in atherosclerotic peripheral arterial

disease. Am J Cardiol 200188:43J-47J.


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Treatment(1 of 2)

Therapy for PAD is focused on prevention of cardiovascular events, amelioration of claudication symptoms, and

prevention of skin breakdown, wound formation, or infection. A multidisciplinary task force was established to provide

guidelines for the management of patients with PAD a brief summary of their recommendations follows.5

The primary method to prevent adverse cardiovascular events in patients with PAD is risk factor modification.

Smoking Cessation

Cigarette smoking is the risk factor most strongly correlated with PAD. It follows that smoking cessation offers significant

opportunity to improve limb as well as general cardiovascular outcomes. In one study, smoking cessation improved

mean treadmill walking distance by 40% at 10 months compared with patients who failed to quit smoking. 10 In two

studies of patients undergoing vascular surgery, smoking cessation (or reduction) improved 3-year survival from 40% to

65-67%.11,12

Lipid-Lowering Therapy

Lipid-lowering therapy to a target low-density lipoprotein (LDL)


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improved by 3 blocksa 130% improvementcompared with baseline.

In the CLEVER (Claudication: Exercise Versus Endoluminal Revascularization) trial, 111 patients with claudication and

aortoiliac PAD were randomized to treatment with a supervised exercise program, endovascular therapy with stenting, or

optimal medical care (including cilostazol pharmacotherapy). At 6 months, the primary endpoint-improvement in peak

walking time-was greatest for those enrolled in a supervised exercise program (5.8 4.6 minutes more than baseline),

intermediate for those who underwent stenting (3.7 4.9), and least for those treated with optimal medical care (1.2

2.6). Interestingly, the quality of lifemeasured using the Walking Impairment Questionnaire and Peripheral Artery

Questionnairewas improved with both supervised exercise and stenting (compared with optimal medical care), but

was more improved with stenting than with exercise.

While the CLEVER study demonstrates the important roles for exercise therapy and endovascular therapy in themanagement of patients with aortoiliac disease, the generalizability of the findings warrants further examination. The

study involved a small and highly selected cohort of patients, which may not reflect real world clinical scenarios. The

discrepancy between the treadmill and quality of life outcomes may cloud the trial's potential impact on practice.

Supervised exercise programs are not currently reimbursed for patients with PAD under Medicare guidelines. Longer-

term follow-up will be required to assess the durability of these treatment strategies.16

A variety of mechanisms have been proposed to explain how exercise improves claudication, including:

Vascular angiogenesis (collateral vessel development).

Increased exercise pain tolerance.

Improved muscle energy metabolism.

Improved endothelial function.

Decreased inflammation and free radical formation in muscle.

Reduced blood viscosity and red blood cell aggregation.


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Treatment(2 of 2)

Pharmacotherapy for Claudication

Medical therapy also may improve symptoms of claudication. The current Food and

Drug Administration (FDA)-approved therapies for claudication include cilostazol and

pentoxifylline. Cilostazol is a phosphodiesterase inhibitor (PDE-3), which promotes

vasodilatation and inhibits platelet aggregation. In clinical trials, cilostazol

statistically improved IC distance after 12 weeks of therapy compared with placebo(from baseline 71.2 minutes to post-treatment 112.5 minutes, compared with 77.7

minutes to 84.6 minutes, respectively p = 0.007). Absolute claudication distance

also was improved (141.9 minutes to 231.7 minutes, compared with 168.6 minutes

to 152.1 minutes, respectively p = 0.002). Cilostazol generally is perceived to be

more effective than pentoxifylline but bears a black box warning from the FDA for use

in patients with congestive heart failure.17

As described previously in the CLEVER trial, cilostazol-administered to those

patients receiving optimal medical care-did not engender equivalent improvement in

peak walking time or quality of life compared with either supervised exercise

programs or endovascular therapy.16 Pentoxifylline was shown to have only modest

improvement in absolute walking distance compared with a placebo control in a

meta-analysis of 11 clinical trials18 as a result, pentoxifylline receives only a ClassIIb indication for therapy for IC in the ACC/AHA PAD and TASC-II guidelines.

Endovascular Therapy

In select individuals, revascularization also may also be considered for the treatment

of PAD. In cases of severe limb ischemia, such as CLI where the viability of the limb

is threatened, the indication for revascularization may be clear. Perfusion to the foot

is typically very poor, with ankle pressures


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Acute Limb Ischemia

Acute limb ischemia (ALI) is an uncommon manifestation of PAD but carries substantial risk of morbidity and mortality.

ALI is characterized by the six Ps of pain, pallor, pulselessness, paresthesia, paralysis , and poikilot hermia (coolnes s)

and may represent imminent threat to the extremity. Mechanistically, ALI often may result from acute embolic arterial

occlusion. Emboli may come from a central cardiac source, such as with atrial fibrillation or paradoxical embolization, in

the context of a hypercoagulable state, or traveling from a more proximal aneurysm, such as in the aorta or the popliteal

artery.

The onset of ALI represents a true emergency, equivalent to a "leg attack." If the limb remains ischemic for >6 hours,permanent ischemic sensory and motor loss may ensue. Following diagnosis of ALI, heparin infusion should be initiated

immediately while plans for revascularization are under way.

Invasive angiography, with plans to pursue endovascular revascularization if feasible, is a standard first-line approach.

Catheter-directed thrombolysis with tissue plasminogen activator may be considered if thrombus burden is substantial.

Suction thrombectomy and rheolytic thrombectomy are adjunctive endovascular approaches to reduce thrombus burden

and may be used in conjunction with angioplasty and stenting. In some cases, surgical thrombectomy or bypass may be

required.

Following reperfusion, the limb should be monitored closely for edema and tissue swelling causing compartment

syndrome. In severe cases, swellingconstrained within fascial compartments of the legmay lead to permanent nerve

injury with sensory and motor loss if surgical fasciotomy is not performed.


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References

1. Criqui MH, Langer RD, Fronek A, et al. Mortality over a period of 10 years in patients with peripheral arterial

disease. N Engl J Med 1992326:381-6.

2. Hiatt WR, Hoag S, Hamman RF. Effect of diagnostic criteria on the prevalence of peripheral arterial disease. The

San Luis Valley Diabetes Study. Circulation 199591:1472-9.

3. Hirsch AT, Criqui MH, Treat-Jacobson D, et al. Peripheral arterial disease detection, awareness, and treatment in

primary care. JAMA 2001286:1317-24.

4. Selvin E, Erlinger TP. Prevalence of and risk factors for peripheral arterial disease in the United States: results

from the National Health and Nutrition Examination Survey, 1999-2000. Circulation 2004110:738-43.

5. Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 guidelines for the management of patients with peripheral

arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): executive summary a collaborative

report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular

Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and

the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of

Patients With Peripheral Arterial Disease) endorsed by the American Association of Cardiovascular and

Pulmonary Rehabilitation National Heart, Lung, and Blood Institute Society for Vascular Nursing TransAtlantic

Inter-Society Consensus and Vascular Disease Foundation. J Am Coll Cardiol 200647:1239-312.

6. Norgren L, Hiatt WR, Dormandy JA, Nehler MR, Harris KA, Fowkes FG. Inter-Society Consensus for the

Management of Peripheral Arterial Disease (TASC II). J Vasc Surg 200745 Suppl S:S5-67.

7. Weitz JI, Byrne J, Clagett GP, et al. Diagnosis and treatment of chronic arterial insufficiency of the lower

extremities: a critical review. Circulation 199694:3026-49.

8. Criqui MH. Systemic atherosclerosis risk and the mandate for intervention in atherosclerotic peripheral arterialdisease. Am J Cardiol 200188:43J-47J.

9. Hirsch AT, Murphy TP, Lovell MB, et al. Gaps in public knowledge of peripheral arterial disease: the first national

PAD public awareness survey. Circulation 2007116:2086-94.

10. Quick CR, Cotton LT. The measured effect of stopping smoking on intermittent claudication. Br J Surg 198269

Suppl:S24-6.

11. Faulkner KW, House AK, Castleden WM. The effect of cessation of smoking on the accumulative survival rates of

patients with symptomatic peripheral vascular disease. Med J Aust 19831:217-9.

12. Lassila R, Lepantalo M. Cigarette smoking and the outcome after lower limb arterial surgery. Acta Chir Scand

1988154:635-40.

13. MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: a

randomised placebo-controlled trial. Lancet 2002360:7-22.

14. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial

infarction, and stroke in high risk patients. BMJ 2002324:71-86.

15. Effects of ramipril on cardiovascular and microvascular outcomes in people with diabetes mellitus: results of theHOPE study and MICRO-HOPE substudy. Heart Outcomes Prevention Evaluation Study Investigators. Lancet

2000355:253-9.

16. Murphy TP, Cutlip DE, Regensteiner JG, et al. Supervised Exercise Versus Primary Stenting for Claudication

Resulting From Aortoiliac Peripheral Artery Disease: Six-Month Outcomes From the Claudication: Exercise Versus

Endoluminal Revascularization (CLEVER) Study. Circulation 2012125:130-9.

17. Dawson DL, Cutler BS, Meissner MH, Strandness DE, Jr. Cilostazol has beneficial effects in treatment of

intermittent claudication: results from a multicenter, randomized, prospective, double-blind trial. Circulation

199898:678-86.

18. Hood SC, Moher D, Barber GG. Management of intermittent claudication with pentoxifylline: meta-analysis of

randomized controlled trials. CMAJ 1996155:1053-9.

19. Adam DJ, Beard JD, Cleveland T, et al. Bypass versus angioplasty in severe ischaemia of the leg (BASIL):

multicentre, randomised controlled trial. Lancet 2005366:1925-34.

20. Schillinger M, Sabeti S, Loewe C, et al. Balloon angioplasty versus implantation of nitinol stents in the superficialfemoral artery. N Engl J Med 2006354:1879-88.

21. Dorros G, Jaff MR, Dorros AM, Mathiak LM, He T. Tibioperoneal (outflow lesion) angioplasty can be used as

primary treatment in 235 patients with critical limb ischemia: five-year follow-up. Circulation 2001104:2057-62.

22. Lipsitz EC, Veith FJ, Ohki T. The value of subintimal angioplasty in the management of critical lower extremity

ischemia: failure is not always associated with a rethreatened limb. J Cardiovasc Surg (Torino) 200445:231-7.


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Natural History(2 of 2)

Other Small Vessel Disease States

Many other systemic conditions may result in obstruction of the small vessels in the upper extremity. Connective tissue

disorders such as CREST syndrome, scleroderma, systemic lupus erythematosus, and rheumatoid arthritis may

promote small vessel vasculitis. In these cases, the vasculitis is managed by treating the underlying systemic

inflammatory condition, typically with immunosuppressant therapy or corticosteroids.

Hypercoagulable states, such as antiphospholipid antibody syndrome, lupus anticoagulant, heparin-induced

thrombocytopenia, and others, may result in occlusion of small vessels. Treatment may include systemic anticoagulation

or antithrombotic therapy. Blood dyscrasia, such as cryoglobulinemia (hepatitis C) and myeloproliferative disorders, also

may lead to vasculitis and occlusion of small vessels. Therapy typically is focused on treatment of the underlying

systemic illness.

Thoracic Outlet Syndrome

TOS results from compression of the nerve or vascular structures that exit the superior outlet of the thorax. The brachial

plexus exits the scalene triangle (between the anterior and middle scalene muscles) and then passes over the first rib

and under the clavicle through the costoclavicular space. The brachial plexus is joined in the costoclavicular space by the

subclavian artery and vein. The nerve and vascular structures particularly may be subjected to compression in the

costoclavicular space in patients who have a cervical first rib.16

Most cases (95%) of TOS involve impingement of the brachial plexus, and 5% involve vascular compromise. The

symptoms of TOS often are provoked by arm activity, particularly when the arm is raised above the head, and

characterized by ache and fatigue. Many cases of TOS are characterized by symptoms due to superimposed Raynaud's

disease. TOS cases with arterial involvement are rare but may have severe consequences. Initially, symptoms may be

mild due to gradual development of collaterals. Over time, stenosis and poststenotic dilatation may occur, and symptoms

may worsen abruptly due to thrombosis proximally or distal embolization.17

Evaluation of patients with TOS should include bilateral arm blood pressures and a pulse examination at rest and with

provocative maneuvers. Adson's maneuver involves abduction and external rotation of the arm and is potentiated further

by turning the head to the opposite direction of the arm evaluated and having the patient take a deep breath. During the

maneuver, the ipsilateral arm pulses should diminish. Auscultation also may disclose a bruit due to dynamic subclavian

stenosis during provocative maneuvers. TOS maneuvers may be positive in 15% of patients with no symptoms

conversely, maneuvers may be negative in patients with known TOS.

16,17

Radiography should be performed to exclude a cervical first rib. Angiography should be performed in patients with TOS

who have developed peripheral emboli or in patients being considered for surgery.

Therapy for TOS includes physical therapy to address posture and minimize nerve and vascular impingement in the

thoracic outlet. Surgery may be considered, particularly in cases of a cervical rib, where rib resection may reduce vessel

entrapment in the costoclavicular space.

Aneurysm

The natural history, prognosis, and treatment strategies for aneurysms in the upper extremity vary based on the location

and etiology of the lesion. In the subclavian artery, aneurysms may develop from a variety of different causes. In TOS,

recurrent impingement of the subclavian artery may lead to stenosis with poststenotic dilatation. In many cases, release

of the vessel impingement-most often resection of a cervical rib-may promote remodeling and resolution of the

poststenotic dilatation. In cases where aneurysmal dilatation continues to progress, resection of the aneurysm with

placement of an interposition graft (autologous saphenous vein) is required.

Subclavian artery aneurysms also may be caused by atherosclerosis or trauma. In certain lesions, PTFE-covered stent

grafts may be considered for aneurysm exclusion using endovascular technique. In subclavian artery aneurysms due to

inflammatory vasculitis (giant cell arteritis, Takayasu's arteritis), treatment is focused on management of the underlying

inflammation with corticosteroids or immunosuppressive therapy.

In patients with an aberrant RSA (arteria lusoria), which is a congenital vascular anomaly where the RSA arises from the

aorta distal to the take-off of the LSA, 60% of patients may develop an aneurysmal dilatation of the vessel origin, termed a

diverticulum of Kommerell. The artery courses between the esophagus and the spine in certain cases, vascular

impingement of the esophagus or of the recurrent laryngeal nerve may lead to dysphagia and hoarseness, termed

dysphagia lusoria. Patients with Kommerell's diverticulum and dysphagia lusoria are prone to aneurysmal rupture and

may benefit from prophylactic surgical repair.18,19


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Axillary artery aneurysms most commonly are due to traumatic injury. The most common mechanism is the use of

crutches, causing repetitive axillary trauma. Other repetitive trauma, such as the occupational use of a hammer or

jackhammer or involvement in professional sports with repetitive aggressive motion of the wrist (baseball pitching, golf),

may result in hypothenar hammer syndrome, characterized by ulnar arterial injury with stenosis or aneurysm formation.

Raynaud's Disease

Raynaud's disease is a primary vasospastic process involving the small vessels of the upper extremity and represents

the most common form of upper extremity PAD. Upon exposure to cold weather or stress, the hand and fingers develop

characteristic tricolored progression of changes in appearance: initially the affected digits blanch to a very pale white

color then the color becomes dusky blue and with rewarming and compensatory capillary vasodilatation, the color

becomes red. The diagnosis may be confirmed with cold water immersion testing, where the color changes may beobserved and the hand is slow to warm. Plethysmography also may demonstrate the development of peaked velocities

during periods of vasospasm in the affected digits.

Treatment of Raynaud's includes preventive strategies such as cold avoidance, wearing gloves, and reducing stress.

Calcium channel blockers and alpha adrenergic blocking agents may be helpful to reduce vasospasm. Raynaud's

syndromea secondary phenomenonmay occur in response to local conditions, such as TOS or local trauma, as well

as with systemic issues, such as connective tissue disorders (systemic lupus erythematosus, scleroderma, rheumatoid

arthritis), or as a side effect from certain medications or drug use (beta-blockers, ergotamine-containing medications,

illicit substances).20

Reflex sympathetic dystrophy-or complex regional pain syndrome (CRPS)-may involve a complex interplay between the

sympathetic nervous system and the microcirculation of the distal portion of the affected limb. While specific

mechanisms remain unclear, neurogenic inflammation and inhibition of local sympathetic tone during the acute phase of

CRPS promote regional vasodilatation. Subsequently, the local rise in sympathetic tone causes vasoconstriction during

the chronic phase of the disease. The associated skin warming during the acute phase and vasoconstriction in the

chronic phase are classic stigmata of CRPS.21


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Renal Stent Placement Procedural Outcomes

Table 6

Reproduced with permission from Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 guidelines for the management of patients with

peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): executive summary a collaborative report from the

American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society

for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee

to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease) endorsed by the American Association of Cardiovascular

and Pulmonary Rehabilitation National Heart, Lung, and Blood Institute Society for Vascular Nursing TransAtlantic Inter-Society Consensus and

Vascular Disease Foundation. J Am Coll Cardiol 200647:1239-312.


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Computed Tomography Angiographic Image of Visceral Artery Anatomy Demonstrating Diseased Origins

Figure 3

IMA = inferior mesenteric artery SMA = superior mesenteric artery.


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Imaging Tests for Visceral Artery Disease

Table 1

CT = computed tomography MR = magnetic resonance SMA = superior mesenteric artery USG = ultrasonography.


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9 peripheral artery disease

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